Fig. 1: Change in the proportion of “wild type” PRNP homozygotes among older age Table Mesa mule deer. | Communications Biology

Fig. 1: Change in the proportion of “wild type” PRNP homozygotes among older age Table Mesa mule deer.

From: Apparent stability masks underlying change in a mule deer herd with unmanaged chronic wasting disease

Fig. 1

The proportion of Table Mesa mule deer (Odocoileus hemionus) homozygous for serine (S) at PRNP codon 225 (225SS), or “wild type”, in 1–2-year-old vs. older (≥3 years old) age cohorts sampled in 2005 or in 2018–2019 (grey bars) and corresponding prion infection prevalence (per cent of sampled deer testing positive) among 225SS deer in those cohort groups (red dashes). Individuals expressing at least one phenylalanine at codon 225 comprised the balance of deer sampled within each cohort; such individuals tend to have lower probability of prion infection and show slower disease progression8,13,16,17,18,19. The high proportion of 225SS deer (~0.89) among the cohort of 1- or 2-year-old deer (n = 28) indicate that their recruitment into the herd had not changed measurably between the two sampling periods. However, by 2018–2019 prion infection and subsequent disease-associated attrition of the relatively susceptible infected 225SS individuals ~2 years later manifested as a lower proportion of 225SS deer among the cohort of deer aged 3 years or older (n = 71) as compared to the younger cohort (two-tailed Fisher’s exact test P = 0.042). Genetic data from deer sampled at Table Mesa in 20055 (n = 32 in 1–2-year-old cohort, n = 60 in ≥3-year-old cohort) are included for comparison to illustrate the relatively recent emergence of this pattern. Capped vertical lines are 95% binomial confidence intervals.

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